The mechanism by which specific pathogenic bacteria evades killing by the serum complement system has been studied. Initial studies with a serum resistant strain of Salomenella minnesota showed that the organism totally consumed terminal complement components through C9 whereas a serum sensitive mutant of the above parent strain consumed only small amounts of the terminal components. Studies using purified, radiolabeled terminal components indicated that a complement membrane attack complex (C5b-9) formed on the surface of the serum resistant strain. However the C5b-9 complex was shed from the surface and was not bactericidal because it did not insert into hydrophobic portions of the outer membrane. In contrast, the C5b-9 complex was inserted by stable, hydrophobic interactions into the outer membrane of the serum sensitive strain. Subsequent studies with rough and encapsulated serum resistant S. pneumoniae showed that both strains caused substantial consumption of terminal complement components from human serum. Relatively stable deposition of C5b-9 on the bacterial cell wall was demonstrated for both strains. Therefore, in serum resistant S. pneumoniae, there is an apparent failure of the attached complex to penetrate the thick peptidoglycan layer.